ESM1通过调控PI3K/AKT信号通路促进宫颈癌细胞增殖和侵袭

ESM1 promotes the proliferation and invasion of cervical cancer cells by regulating the PI3K/AKT signaling pathway

目的探讨ESM1在宫颈癌组织中的表达情况及对人宫颈癌细胞增殖和侵袭的影响,并识别可能机制。方法利用GEPIA数据库分析宫颈癌组织及正常组织中ESM1表达情况;利用Kaplan Meier plotter在线分析工具分析ESM1的表达和患者预后的相关性;将ESM1小干扰RNA及其阴性对照分别转染进宫颈癌细胞系。CCK-8,EdU和Transwell实验检测ESM1对人宫颈癌细胞增殖和侵袭的影响。使用Western blot实验检测ESM1对宫颈癌细胞中p-PI3K和p-AKT蛋白表达的影响。结果GEPIA数据库显示ESM1在宫颈癌组织中表达水平显著高于正常宫颈组织(P<0.05)。ESM1高表达和宫颈癌患者预后较差显著相关(P<0.05)。敲低ESM1可显著抑制宫颈癌细胞增殖和侵袭能力(P<0.05)。此外,敲低ESM1可抑制宫颈癌细胞系中p-PI3K和p-AKT蛋白的表达(P<0.05)。结论ESM1在宫颈癌组织中高表达,其可通过调控PI3K/AKT信号通路促进宫颈癌细胞增殖和侵袭。

Objective To study the expression of ESM1 in cervical cancer tissues and the effect of ESM1 on the proliferation and invasion of cervical cancer cells,as well as its possible mechanism.Methods The expression of ESM1 in cervical cancer tissues and normal tissues was analyzed by using the GEPIA database.Kaplan Meier plotter was used to analyze the relationship between ESM1 expression and the prognosis of cervical cancer patients.Small interfering RNA targeting ESM1 and its negative control was transfected into the cervical cancer cell lines,respectively.CCK-8,EdU and Transwell assays were used to detect the effects of ESM1 on the proliferation and invasion of cervical cancer cells.Western blot was used to detect the effect of ESM1 on p-PI3K and p-Akt protein expression in cervical cancer cells.Results GEPIA database showed that the expression level of ESM1 in cervical cancer tissues was significantly higher than that in normal cervical tissues(P<0.05).The high expressions of ESM1 was significantly correlated with the poor prognosis of cervical cancer patients(P<0.05).Knockdown of ESM1 significantly inhibited the proliferation and invasion of cervical cancer cells(P<0.05).Inaddition,knockdown of ESM1 can inhibit the expressions of p-PI3K and p-Akt proteins in cervical cancer cell lines.Conclusion ESM1 is upregulatedin cervical cancer tissues,and ESM1 can promote the proliferation and invasion of cervical cancer cells by regulating PI3K/AKT signaling pathway.